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Polarity in intracellular calcium signaling
Author(s) -
Petersen Ole H.,
Burdakov Denis,
Tepikin Alexei V.
Publication year - 1999
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(199910)21:10<851::aid-bies7>3.0.co;2-f
Subject(s) - endoplasmic reticulum , microbiology and biotechnology , cholecystokinin , intracellular , cytosol , inositol , acetylcholine , calcium signaling , chemistry , calcium , stimulation , calcium in biology , organelle , acinar cell , biology , biophysics , endocrinology , biochemistry , pancreas , receptor , organic chemistry , enzyme
The concentration of free calcium ions (Ca 2+ ) in the cytosol is precisely regulated and can be rapidly increased in response to various types of stimuli. Since Ca 2+ can be used to control different processes in the same cell, the spatial organization of cytosolic Ca 2+ signals is of considerable importance. Polarized cells have advantages for Ca 2+ studies since localized signals can be related to particular organelles. The pancreatic acinar cell is well‐characterized with a clearly polarized structure and function. Since the discovery of the intracellular Ca 2+ ‐releasing function of inositol 1,4,5‐trisphosphate (IP 3 ) in the pancreas in the early 1980s, this cell has become a popular study object and is now one of the best‐characterized with regard to Ca 2+ signaling properties. Stimulation of pancreatic acinar cells with the neurotransmitter acetylcholine or the hormone cholecystokinin evokes Ca 2+ signals that are either local or global, depending on the agonist concentration and the length of the stimulation period. The nature of the Ca 2+ transport events across the basal and apical plasma membranes as well as the involvement of the endoplasmic reticulum (ER), the nucleus, the mitochondria, and the secretory granules in Ca 2+ signal generation and termination have become much clearer in recent years. BioEssays 21:851–860, 1999. © 1999 John Wiley & Sons, Inc.